Trichloroethylene estimating exposures

Biological monitoring for recent, as opposed to more remote, exposure to tetrachloroethylene has also been performed by measuring concentrations of tetrachloroethylene and its principal metabolite, TCA, in blood and urine. However, TCA is not specific fortetrachloroethylene because it is also produced from the metabolism of trichloroethylene and 1,1,1-trichloroethane (Monster 1988). In a study of occupationally exposed individuals, measurements of tetrachloroethylene and TCA in the blood 15-30 minutes after the end of the workday at the end of the week were judged to be the best parameters for estimating exposure to the chemical. The best noninvasive method for determining tetrachloroethylene exposure was to measure the concentration of the parent compound in exhaled air. After exposure to a... 

It is estimated that concentrations of 3000 ppm cause unconsciousness in less than 10 minutes (39). Anesthetic effects have been reported at concentrations of 400 ppm after 20-min exposure. Decrease in psychomotor performance at a trichloroethylene concentration of 110 ppm has been reported in one study (33), whereas other studies find no neurotoxic effects at concentrations of 200 ppm (40—43). 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been made for trichloroethylene. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based on noncancer health effects only and do not reflect a consideration of carcinogenic effects. MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. 

Monte Carlo simulation, an iterative technique which derives a range of risk estimates, was incorporated into a trichloroethylene risk assessment using the PBPK model developed by Fisher and Allen (1993). The results of this study (Cronin et al. 1995), which used the kinetics of TCA production and trichloroethylene elimination as the dose metrics relevant to carcinogenic risk, indicated that concentrations of 0.09-1.0 pg/L (men) and 0.29-5.3 pg/L (women) in drinking water correspond to a cancer risk in humans of 1 in 1 million. For inhalation exposure, a similar risk was obtained from intermittent exposure to 0.07-13.3 ppb (men) and 0.16-6.3 ppb (women), or continuous exposure to 0.01-2.6 ppb (men) and 0.03-6.3 ppb (women) (Cronin et al. 1995). 

This study, like that of Fisher and Allen (1993), incorporated a linear multistage model. However, the mechanism of trichloroethylene carcinogenicity appears to be non-genotoxic, and a non-linear model (as opposed to the linearized multistage model) has been proposed for use along with PBPK modeling for cancer risk assessment. The use of this non-linear model has resulted in a 100-fold increase in the virtually safe lifetime exposure estimates (Clewell et al. 1995). 

The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1981 to 1983, estimated that 401,000 workers employed at 23,225 plant sites were potentially exposed to trichloroethylene in the United States (NOES 1990). The NOES database does not contain information on the frequency, concentration, or duration of exposures the survey provides only estimates of workers potentially exposed to chemicals in the workplace. 

Exposure Levels in Humans. This information is necessary for assessing the need to conduct health studies on these populations. Trichloroethylene has been detected in human body fluids such as blood (Brugnone et al. 1994 Skender et al. 1994) and breast milk (Pellizzari et al. 1982). Most of the monitoring data have come from occupational studies of specific worker populations exposed to trichloroethylene. More information on exposure levels for populations living in the vicinity of hazardous waste sites is needed for estimating human exposure. 

Nomiyama K. 1971. Estimation of trichloroethylene exposure by biological materials. Int Arch Arbeitsmed 27 281. 

Trichloroethylene (TCE) is the most common and abundant pollutant in ground-water in the United States. It is primarily used as a solvent to remove grease fiom metal parts, as a solvent for extraction of waxes, oil, fats, tar, and in several consumer products such as paints, carpet cleaning fluid, etc. It is estimated that between 9% and 34% of drinking water supply sources are contaminated with TCE. Several epidemiological studies link TCE exposure to health problems related to congenital heart disease, spontaneous abortion, cancer, etc. 

Both of these approaches allow for assessment of systemic absorption by not conducting complete mass balance studies (e.g., expired air to catch absorbed compound metabolized to COj or HjO expired end products). In vivo dermal absorption studies not taking into account other routes of excretion must be interpreted with caution. One extension of this mass balance excretory analysis is to assess dermal absorption by only monitoring the primary excretory route for the compound studied. Dermal bioavailability has been assessed in exhaled breath using real-time ion trap mass spectrometry to track the uptake and ehmination of compounds (e.g., trichloroethylene) from dermal exposure in humans and rats (Poet et al., 2000). A physiologically based pharmacokinetic model can be used to estimate the total bioavailability of compoimds. The same approach was extended to determine the dermal uptake of volatile chemicals imder non-steady-state conditions using real-time breath analysis in rats, monkeys, and humans (Thrall et al., 2000). 

Characterization of these hazards is often difficult. Important considerations include the potency of the agent, the route of exposure, the level and temporal pattern of exposure, genetic susceptibility, overall health status, and life-style factors that may alter individual sensitivities (eg, alcohol consumption may cause degreaser"s flush in workers exposed to trichloroethylene). Despite their value in estimating the likelihood and potential severity of an effect, quantitative measurements of the level of exposure are not often available. 

Showering or bathing with contaminated water can also result in tetrachloroethylene exposure. Rao and Brown (1993) describe a combined PBPK exposure model that estimates brain and blood levels of tetrachloroethylene following a 15-minute shower or 30-minute bath with water containing 1 mg tetrachloroethylene/L. The PBPK model is described further in Section 2.3.5. The exposure model assumed that the shower or bath would use 100 L of water, the air volume in the shower stall or above the bath tub was 3 m, and the shower flow rate was 6.667 L/minute. The exposure model was validated with data for chloroform and trichloroethylene, but not tetrachloroethylene. Using this model, Rao and Brown (1993) estimated that shower air would contain an average of 1 ppm and that the air above the bathtub would contain an average of 0.725 ppm if the water contained 1 mg tetrachloroethylene/L. 

Exit Solvent Concentration 3.8 ppm (estimated) 10 ppm (exposure limit for trichloroethylene)... 

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